A Study On The Relationship Between Apoptosis And NF-κ B Activation Of Leukemia And Lymphoma Induced By Arsenic Trioxide

objectives the purpose of this study was to investigate the efficacy ofarscnic triOXidc(As203J in inducing apoptosis of Raji,E6-1,K562-n,K562-n/VCR in vitro,respectivclv.The effect of dexamethasone combined with As203 on the apoptosis andthe activation of NF—κBwas studied in Raji and K562-n cell lines.It was alsoobservcd that the fluctuation 0f MMP9 an I VEGF according to the variation of theactivity of NF—κB.Methods The apoptosis of the four cell lines induced byAs203solution of different concentrations were studied with cell morphologv,WST,DNA—ladder and flow cytometry.Fluctuation of NF—κB,MMP9 and VEGFof Rail and J K562·11 was detected by immunohistochemistry.Results We found thatthere was significant difference of IC50 between Raji and E6—1,whereas,nosignificant difference between K562.n a11d K562'n/VCR cell lines.As203 couldinduce the apoptosis of Raji,E6—1,K562.n,K562一nNCR cell lines in a time anddose dependent manner in vitro.The apoptosis and activation of NF—κB0f Raji andK562一n cells could be induced by As203.Dexamethasome increased significantlvthc apoptosis induced by As203,meanwhile,it suppressed activation of NF—κB ofRaji and K562一n cells induced by As203.There was a positive correlation betweenMMP9,VEGF and NF-κB. Conclusions Raji cell line was more susceptible toAs203 than E6—1.As201 had a pronounced effect on K562一nNCR,which had acharacteristics of multidrug resistance.As203 could inducc apoptosis of Raji andK562一n cells,activate NF.K B and up—regulate expression 0f MMP9 and VEGEThe mechanism of in enhanced apoptosis of Raji and K562 . n cells bvdexamethasome may be related to suppressing activation of NF— κB anddown—regulating expression of MMP9 and VEGF...